摘要
目的:神经胶质细胞介导的炎性反应与中枢神经系统多种病理过程有关,本研究旨在探讨静脉麻醉药对神经系统炎性损伤可能的保护作用。方法:本研究采用体外原代培养神经胶质细胞,以细菌脂多糖(LPS)诱导神经胶质细胞的炎性反应,实验分为8组:空白对照组(C组)、LPS对照组(L组)、100μmol/L氯胺酮加LPS组(K1组)、1000μmol/L氯胺酮加LPS组(K2组)、30μmol/L丙泊酚加LPS组(P1组)、300μmol/L丙泊酚加LPS组(P2组)、3μmol/L咪唑安定加LPS组(M1组)和30μmol/L咪唑安定加LPS组(M2组),放射免疫法检测神经胶质细胞的炎性介质TNF-α的产生。结果:L组、K1组、K2组、P1组、P2组、M1组和M2组TNF-α较C组明显增高,差异有统计学意义(P<0.05)。K1组和K2组较L组TNF-α的生成减少,差异有统计学意义(P<0.05),P1组、P2组、M1组和M2组与L组比较差异无统计学意义(P>0.05)。结论:氯胺酮可抑制神经胶质细胞的炎性反应中的TNF-α的释放,由此产生一定的抗炎作用。而丙泊酚和咪唑安定对LPS诱导的神经胶质细胞的TNF-α的产生无明显影响。
Objective To investigate the effects of intravenous anesthetics on LPS-induced inflammatory responses of primary cultures of rat glial cells in vitro. Methods The primary cultures of rat glial cells were stimulated with lipopolysaccharide （ LPS ） to produce inflammatory responses. Glial cells were divided into 8 groups （n =4） ： blank control （Group C） , LPS（ Group L） , 100 μmol/L ketamine with LPS （Group K1 ）, 1 000 μmol/L ketamine with LPS （Group K2 ）, 30 μmol/L propofol with LPS （Group P1 ）, 300 μmol/L propofol with LPS （Group P2 ） , 3 μmol/L midazolane with LPS （Group M1 ） , and 30 μmol/L midazolane with LPS （Group M2 ）. TNF-α released into the culture media was measured by radioimmunity assay. Results Compared with the blank control Group C, LPS-induced TNF-α productions in Group L, K1, K2, P1, P2, M1 and M2 increased significantly. The levels of TNF-α in Group K1 and K2 were significantly lower than those in Group L （ P 〈 0.05 ）, but TNF- α productions in Group P1, P2, M1 and M2 were not significantly different as compared with that in Group L. Conlusion Ketamine can reduce LPS- induced TNF- α production of glial cells, thereby inhabiting some of the inflammatory responses. Propofol and midazolam have no effect on the production of TNF-α from LPS-stimulated glial cells.
出处
《中南大学学报（医学版）》
CAS
CSCD
北大核心
2007年第3期413-416,共4页
Journal of Central South University ：Medical Science
基金
国家自然科学基金(30271256)~~
关键词
静脉麻醉药
脂多糖
神经胶质细胞
TNF-Α
intravenous anesthetics
lipopolysaccharide
glial cell
tumour necrosis factor-α
